1. Field of the Disclosure
The present disclosure relates to a method for treating acquired perforating dermatosis. (APD).
2. Description of the Related Art
Acquired perforating dermatosis (APD) describes a group of disorders associated with transepidermal elimination of collagen, elastic tissue, and/or necrotic connective tissue. The disease is acquired in adulthood. Persons having APD typically have certain systemic diseases such as renal failure and diabetes mellitus. The classic four presentations of perforating dermatosis are Kyrle's disease (KD), reactive perforating collagenosis (RPC), perforating folliculitis (PF), and elastosis perforans serpiginosa (EPS). APD can histologically resemble KD, RPC, PF and occasionally EPS. A significant percentage of dialysis patients also present with APD—11% in the British medical literature and ranging from 4.5% to 10% in the American medical literature. APD has also been reported in association with other systemic disorders including lymphoma, pancreas carcinoma, hypothyroidism, hyperparathyroidism, myelodysplastic syndrome, and AIDS.
APD and related disorders are disclosed and described in the literature at the following: (A) Lebwohl M, Berth-Jones, J., Heymann W. R., Coulson, I., Treatment of Skin Disease: Comprehensive Therapeutic Strategies, 3rd ed. Philadelphia: Saunders Elsevier 2010; (B) Kawakami T, Saito R., Acquired Reactive Perforating Collagenosis Associated with Diabetes Mellitus: Eight Cases that Meet Faver's Criteria, Br J Dermatol, March 1999; 140(3): 521-524; (C) Morton C A, Henderson I S, Jones M C, Lowe J G., Acquired Perforating Dermatosis in a British Dialysis Population, Br J Dermatol, November 1996; 135(5): 671-677; (D) Satti M B, Aref A H, Raddadi A A, Al-Ghamdi F A, Acquired Reactive Perforating Collagenosis: A Clinicopathologic Study of 15 Cases from Saudi Arabia, J Eur Acad Dermatol Venereol,. Feburary 2010; 24(2): 223-227; (E) Rapini R P, Herbert A A, Drucker C R, Acquired Perforating Dermatosis. Evidence for Combined Transepidermal Elimination of both Collagen and Elastic Fibers, Arch Dermatol, August 1989; 125(8): 1074-1078; (F) Abe R, Murase S, Nomura Y, et al., Acquired Perforating Dermatosis Appearing as Elastosis Perforans Serpiginosa and Perforating Folliculitis, Clin Exp Dermatol, August 2008; 33(5): 653-654; (G) Haftek M, Euvrard S, Kanitakis J, Delawari E, Schmitt D., Acquired Perforating Dermatosis of Diabetes Mellitus and Renal Failure: Further Ultrastructural Clues to its Pathogenesis, J Cutan Pathol, August 1993; 20(4): 350-355; (H) Hood A F, Hardegen G L, Zarate A R, Nigra T P, Gelfand M C, Kyrle's Disease in Patients with Chronic Renal Failure, Arch Dermatol, February 1982; 118(2): 85-88; (I) Hurwitz R M, Melton M E, Creech F T, 3rd, Weiss J, Handt A., Perforating Folliculitis in Association with Hemodialysis, Am J Dermatopathol, April 1982; 4(2): 101-108; (J) Patterson J W, The Perforating Disorders, J Am Acad Dermatol, April 1984; 10(4): 561-581; (K) Saray Y, Seckin D, Bilezikci B, Acquired Perforating Dermatosis: Clinicopathological Features in Twenty-Two Cases, J Eur Acad Dermatol Venereol, July 2006; 20(6): 679-688; (L) Mehregan A H, Coskey R J, Perforating folliculitis, Arch Dermatol, April 1968; 97(4): 394-399; (M) Cochran R J, Tucker S B, Wilkin J K, Reactive Perforating Collagenosis of Diabetes Mellitus and Renal Failure, Cutis, January 1983; 31(1): 55-58; (N) Bilezikci B, Seckin D, Demirhan B, Acquired Perforating Dermatosis in Patients with Chronic Renal Failure: A Possible Pathogenetic Role for Fibronectin, J Eur Acad Dermatol Venereol, March 2003; 17(2): 230-232; (O) Moed L, Shwayder T A, Chang M W, Cantharidin Revisited: A Blistering Defense of an Ancient Medicine, Arch Dermatol., October 2001; 137(10): 1357-1360; and (P) Pierard-Franchimont C, Pierard G E. Cantharidin-Induced Acantholysis, Am J Dermatopathol, October 1988; 10(5): 419-423.
The pathophysiology behind APD is unclear. It has been postulated that mechanical trauma, such as chronic rubbing from pruritus, diabetes mellitus, and renal failure, causes epithelial hyperplasia, follicular hyperkeratosis, and degeneration of connective tissue in the dermis. Diabetic vasculopathy and oxidation injury may also lead to dermal necrosis. Some APD patients on peritoneal or hemodialysis have developed lesions upon initiating dialysis. The role of increased serum fibronectin in patients with diabetes mellitus and uremia may also be a factor as increased fibronectin has been found in the skin at the sites of perforating lesions.
Many treatments have been proposed for treating APD. Success has varied. In general, treatment efforts have been unsatisfactory, and definitive resolution of existing lesions has been difficult to achieve.
First-line therapies for perforating dermatosis include tretinoin 0.1% (topical), broadband UVB (ultraviolet B), and narrowband UVB. Second-line therapies include allopurinol, PUVA (psoralens +ultraviolet A), and acitretin. Third-line therapies include 0.5% phenol with 10% glycerine in sorbolene, doxycycline (oral), surgical debridement, and transcutaneous electrical nerve stimulation. Topical steroids have also been employed.
It would be desirable to have an effective treatment for APD. It would also be desirable to have a treatment that is applied topically and is effective with respect to reduction/amelioration of symptoms and clearance of lesions.